星形细胞上调基因-1（AEG-1）可被脂多糖诱导，作为 toll 样受体 4（TLR4）配体，调节 TLR4 信号通路。
Astrocyte elevated gene-1 (AEG-1) is induced by lipopolysaccharide as toll-like receptor 4 (TLR4) ligand and regulates TLR4 signalling.
机构信息
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.
出版信息
Immunology. 2009 Sep;128(1 Suppl):e700-6. doi: 10.1111/j.1365-2567.2009.03063.x. Epub 2009 Feb 9.
Abstract
Astrocyte elevated gene-1 (AEG-1) is induced by human immunodeficiency virus 1 (HIV-1) infection and involved in tumour progression, migration and invasion as a nuclear factor-kappaB (NF-kappaB) -dependent gene. The involvement of AEG-1 on lipopolysaccharide (LPS) -induced proinflammatory cytokine production was examined. AEG-1 was induced via NF-kappaB activation in LPS-stimulated U937 human promonocytic cells. AEG-1 induced by LPS subsequently regulated NF-kappaB activation. The prevention of AEG-1 expression inhibited LPS-induced tumour necrosis factor-alpha and prostaglandin E(2) production. The AEG-1 activation was not induced by toll-like receptor ligands other than LPS. Therefore, AEG-1 was suggested to be a LPS-responsive gene and involved in LPS-induced inflammatory response.
摘要
星形细胞上调基因-1（AEG-1）可被人类免疫缺陷病毒 1（HIV-1）感染诱导，并作为核因子-κB（NF-κB）依赖性基因参与肿瘤的进展、迁移和侵袭。本研究旨在探讨 AEG-1 是否参与脂多糖（LPS）诱导的促炎细胞因子产生。LPS 刺激 U937 人单核细胞前体细胞后通过 NF-κB 激活诱导 AEG-1。LPS 诱导的 AEG-1 随后调节 NF-κB 激活。抑制 AEG-1 表达可抑制 LPS 诱导的肿瘤坏死因子-α和前列腺素 E2 的产生。除 LPS 以外的 Toll 样受体配体不能诱导 AEG-1 的激活。因此，AEG-1 可能是 LPS 反应性基因，并参与 LPS 诱导的炎症反应。
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